There's a "headbanging" joke here, but I just can't quite put it together.

---

So nobody's decided to try to cash in on my offer of an e-high-five, eh? I'm probably too impatient. Anyways, here's what I missed.

If you look at this table, the only oil listed that has more long-chain omega-6 than long-chain omega-3 is cottonseed. A naive reading of this would indicate that if, as Sears argues, we're trying to avoid having an AA:EPA ratio that's too slanted towards AA, all we have to do is avoid cottonseed oil.

This, however, is not necessarily correct. Consider my reference to ALA as a potentially-pertinent substance - it's a short-chain omega-3 that, it appears, is partially converted to our relevant long-chain omega-3s. Could it be that there are analogous short-chain omega-6 fatty acids that the body can convert to arachidonic acid?

Human adults are shown to be capable of conversion of linoleic acid (LA, 18:2 n-6) to arachidonic acid (AA, 20:4 n-6) in vivo. It is confirmed that they can also convert alpha-linolenic acid (LNA, 18:3 n-3) to eicosapentaenoic acid (EPA, 20:5 n-3) and to docosahexaenoic acid (DHA, 22:6 n-3) in vivo.

Said book also makes reference to competition between LA (linoleic acid, 18:2 n-6) and ALA for conversion into AA and EPA/DHA, respectively.

The plot thickens.

Edit: And to confuse things even more, there are reports of gender-based differences.

Increasing alphaLNA intake for a period of weeks to months results in an increase in the proportion of eicosapentaenoic acid (EPA; 20:5n-3) in plasma lipids, in erythrocytes, leukocytes, platelets and in breast milk but there is no increase in docosahexaenoic acid (DHA; 22:6n-3), which may even decline in some pools at high alphaLNA intakes. Stable isotope tracer studies indicate that conversion of alphaLNA to EPA occurs but is limited in men and that further transformation to DHA is very low. The fractional conversion of alphaLNA to the longer chain n-3 PUFA is greater in women which may be due to a regulatory effect of oestrogen. A lower proportion of alphaLNA is used for beta-oxidation in women compared with men.

I was going to start on creatine after the tournament, because I didn't want to wind up in +100kg. The weight classes were merged, so that's a moot point. And then I decided not to start supplementing with it afterwards because:
1) I wasn't in the gym, so what good would it do?
2) Would it damage my brain? I mean, creatine uptake -> water uptake to maintain homeostasis -> swelling -> increased ICP, right?

Well, guess what...

Results demonstrate that chronic administration of creatine ameliorated the extent of cortical damage by as much as 36% in mice and 50% in rats. Protection seems to be related to creatine-induced maintenance of mitochondrial bioenergetics.

Animals fed a 1% Cr-diet were afforded greater neuroprotection than animals fed a 0.5% Cr diet. These results support the idea that a Cr-enriched diet can provide substantial neuroprotection in part by suppressing secondary brain injury.

Although creatine did not attenuate gray matter loss in the NYU cohort, it significantly spared gray matter in the IH cohort with pre-fed and pre & post-fed regimens. Such selective sparing of injured spinal cord gray matter with a dietary supplement yields a promising strategy to promote neuroprotection after SCI.

The administration of creatine to children with TBI improved results in several parameters, including duration of post-traumatic amnesia (PTA), duration of intubation, intensive care unit (ICU) stay, disability, good recovery, self care, communication, locomotion, sociability, personality/behavior and neurophysical, and cognitive function. Significant improvement was recorded in the categories of Cognitive (p < 0.001), personality/behavior (p < 0.001), Self Care (p = 0.029), and communication (p = 0.018) aspects in all patients. No side effects were seen because of creatine administration.

Here, we review the roles of Cr and Cr-related enzymes and consider the potential
value of supplementation with Cr, a potent neuroprotective substance. As a hypothesis, we consider whether Cr, if given at an early time point of the disease, may prevent or delay the course of AD-related neurodegeneration.

Yeah, I've been following that story with some interest. Worst head trauma I'd had (prior to this, I guess) was while skiing. Kind of funny how all this stuff about head trauma comes out immediately after I get my eggs scrambled, eh?

At least people are paying attention to it now.

---

Originally Posted by honesty

Given that, whats your view on the anabolic diet and creatine supplements. I guess you're going to get increased creatine on the AD anyway from the amount of red meat you're meant to eat.

I'd probably still supplement - I've heard varying numbers as far as how much creatine is actually in cooked meat. I suppose you could probably get away without supplements after you're done loading, but hey, the stuff's dirt cheap.

Also, for anyone waiting on my "verdict" re: fish oils, there are a few problems.

1) I got bloodwork done today, but no AA:EPA ratio, so I'd be working blind.
2) Given that I eat two cans of salmon a day (and have been eating at least one a day for the last year), I'm already getting more EPA/DHA daily than most of my sources recommend supplementing with.
3) There are plenty of studies about EPA/DHA supplementation, but it looks like the people running them are screwing them up in one way or another, because review efforts like Cochrane Collaboration aren't drawing any conclusions based on them.
4) The lipid chemistry governing the conversions between short-chain and long-chain polyunsaturated fatty acids is... well, whether it's not well understood or not in general, it's not well understood by me.

That said, I've still got a container of concentrated EPA/DHA caps from Costco, so I may still give it a shot. Right now, though, it looks like you're better off just eating canned wild Pacific salmon, from both a nutritional (hooray, bonus protein) and financial perspective.

So how does an average serving of, say, canned chunk tuna stack up next to an average serving of canned wild Pacific salmon in regards to daily amount of EPA/DHA? Did you choose wild Pacific salmon because it's got mo' fish oil than other types of canned fish products, or is it just a matter of taste?

So how does an average serving of, say, canned chunk tuna stack up next to an average serving of canned wild Pacific salmon in regards to daily amount of EPA/DHA? Did you choose wild Pacific salmon because it's got mo' fish oil than other types of canned fish products, or is it just a matter of taste?

Oh, and a warning... grocery stores tend to have nearly a 100% markup on cans of salmon over Costco ($7.99/6 cans at last visit)/Wholesale Club ($6.99/6 cans at last visit). Wal-Mart had relatively cheap keta salmon last time I was there ($1.25/can), but keta tends to be lower in fat and blander.

Because "the total concentration of LCPUFA administered was the same for all experiments", the scales of these graphs are a bit misleading for our purposes - the bars are ratios of AA/EPA/DHA vs. the recovered LA or ALA, which themselves are administered such that the total LA+ALA is constant. I'd probably have done a two-dimensional analysis instead (vary both LA and ALA concentrations independently), but that'd probably have made things more expensive.

Still, though, it's interesting to see the in vitro performance of the conversions - the relationship between SCPUFA ingestion and LCPUFA creation is probably greater than linear because of its effects on the competition between LA and ALA.